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• Research Paper Volume 13, Issue 23 pp 25325-25341

  Artesunate treatment ameliorates ultraviolet irradiation-driven skin photoaging via increasing β-catenin expression

  Relevance score: 6.101354

  Liming Tian, Dan Ke, Yi Hong, Chong Zhang, Daizhi Tian, Long Chen, Lirui Zhan, Shiqin Zong

  Keywords: artesunate, skin photoaging, β-catenin, ultraviolet radiation, cell senescence

  Published in Aging on December 9, 2021

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  Objective: Artesunate, a semi-synthetic derivative of artemisinin, exerts various pharmacological activities. Nevertheless, the effects of Art on skin photoaging remain unclear. Herein, we investigated whether Art ameliorated ultraviolet-irradiated skin photoaging in HaCaT cells and mice.

  Methods: To construct skin photoaging cellular models, HaCaT cells were irradiated by UV (UVB, 20mJ/cm²) for 5 days. HaCaT cells were pretreated with three concentrations of Art (1, 5 and 20 μg/ml) for 2 h each day. After 5 days, cell senescence, ROS production, SOD levels, p16^INK4a and β-catenin expression, proliferation and apoptosis were detected in HaCaT cells. Effects of Art on normal cells were investigated. After sh-β-catenin transfection or XAV-939 treatment, HaCaT cells were pretreated with 20 μg/ml Art and irradiated by UVB. After 5 days, skin photoaging was then observed. Furthermore, skin photoaging mouse models were established and the effects of Art and β-catenin silencing on skin photoaging were investigated.

  Results: Art treatment suppressed cell senescence, intracellular ROS production, p16^INK4a expression and apoptosis and promoted proliferation and SOD and β-catenin expression in UVB irradiated HaCaT cells. But Art had no toxic effects on normal cells. Silencing β-catenin by sh-β-catenin or XAV-939 exacerbated UVB irradiation-mediated cell senescence, apoptosis, and ROS production in HaCaT cells, which was ameliorated by Art treatment. The therapeutic effects of Art on skin photoaging were also confirmed in mouse models.

  Conclusions: These findings suggested that Art treatment alleviated UVB irradiation-driven skin photoaging through enhancing β-catenin expression, which offered novel clues for pharmacological activity of Art.

• Research Paper Volume 13, Issue 1 pp 89-103

  Further assessment of Salvia haenkei as an innovative strategy to counteract skin photo-aging and restore the barrier integrity

  Relevance score: 5.9258895

  Veronica Cocetta, Jessica Cadau, Miriam Saponaro, Isabella Giacomini, Stefano Dall’Acqua, Stefania Sut, Daniela Catanzaro, Genny Orso, Giorgia Miolo, Luca Menilli, Andrea Pagetta, Eugenio Ragazzi, Monica Montopoli

  Keywords: skin aging, skin photoaging, Salvia haenkei, skin barrier integrity, wound healing

  Published in Aging on January 8, 2021

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  Skin is the essential barrier of the human body which performs multiple functions. Endogenous factors, in concert with external assaults, continuously affect skin integrity, leading to distinct structural changes that influence not only the skin appearance but also its various physiological functions. Alterations of the barrier functions lead to an increased risk of developing disease and side reactions, thus the importance of maintaining the integrity of the epidermal barrier and slowing down the skin aging process is evident.

  Salvia haenkei (SH) has been recently identified as a potential anti-senescence agent; its extract is able to decrease the level of senescent cells by affecting the IL1α release and reducing reactive oxygen species (ROS) generation.

  In this study, SH extract was tested on human keratinocyte cell line (HaCaT) exposed to stress factors related to premature aging of cells such as free radicals and ultraviolet B radiation. We confirmed that SH acts as scavenger of ROS and found its ability to restore the skin barrier integrity by reinforcing the cytoskeleton structure, sealing the tight junctions and increasing the migration rate of cells.

  Given these results, this work becomes relevant, identifying Salvia haenkei as a compound useful for anti-aging skin treatment in clinical performance.

• Research Paper Volume 12, Issue 21 pp 21273-21289

  The role of Hrd1 in ultraviolet (UV) radiation induced photoaging

  Relevance score: 8.079396

  Yi Jin, Xianye Cheng, Xin Huang, Fan Ding, Sae Rom Lee, Fengdi Wang, Xiaoyi Lu, Dongming Su, Bin Chen

  Keywords: Hrd1, IGF-1R, UV, photoaging, collagen

  Published in Aging on November 9, 2020

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  The purpose of the present study was to evaluate the role of Hrd1 in the ultraviolet (UV) radiation induced photoaging and explore its potential mechanism. The nude mice were exposed to the UVA/UVB irradiation for 10 weeks. The animals were subcutaneously injected with AAV5-NC, Hrd1-shRNA-AAV5, or Hrd1-overexpression-AAV5. The HSF cells were also transfected with Ad-NC, Ad-shRNA-Hrd1, or Ad-Hrd1, and irradiated by UVA/UVB stimulation. The clinical skin samples were harvested for detecting Hrd1 and IGF-1R expressions. As a result, the knockdown of Hrd1 attenuated the histopathological alteration and collagen degradation in UV-induced nude mice. The inhibition of Hrd1 by Hrd1-shRNA-AAV5 and Ad-shRNA-Hrd1 inhibited the Hrd1 expression and promoted IGF-1R, Type I collagen and type III collagen in mice and HSF cells. The overexpression of Hrd1 exerted the reverse effect. The Co-IP assay also indicated the interaction between Hrd1 and IGF-1R. Hrd1-mediated IGF-1R downregulation and collagen degradation were also observed in clinical skin samples. In conclusion, the present results demonstrated that Hrd1 degraded IGF-1R and collagen formation in UV-induced photoaging.

• Research Paper Volume 12, Issue 8 pp 7056-7065

  CO₂ lattice laser reverses skin aging caused by UVB

  Relevance score: 4.624532

  Hongyi Wang, Bingyu Guo, Qiang Hui, Feng Lin, Kai Tao

  Keywords: skin, CO lattice laser ², photoaging, in vitro, in vivo

  Published in Aging on April 20, 2020

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  The carbon dioxide (CO₂) lattice laser has been successfully used to treat facial skin photoaging induced by UV light. In this study, we analyzed the effect of CO₂ lattice laser irradiation on skin photoaging, and investigated the underlying mechanisms. Our results demonstrate that the laser promoted collagen synthesis and proliferation of primary human skin fibroblasts, inhibited cell senescence, and induced expression of superoxide dismutase (SOD) and the signaling protein SMAD3. In addition, this laser reversed cell cycle arrest and fibroblast apoptosis induced by UVB irradiation, and restored fibroblast proliferation inhibited by SMAD3 silencing. Using a rat model of photoaging, our results show that the laser increased collagen expression and dermal thickness, demonstrating that the CO₂ lattice laser has a profound therapeutic effect on photoaged skin. Together, our in vitro and in vivo data show that the CO₂ lattice laser can reverse the skin aging caused by UVB, and indicate that this effect is mediated through SMAD3.

  

  Effect of CO₂ Lattice Laser on Fibroblasts. (A) Cell proliferation analyzed by MTT assay after treatment with 0, 1.25, 3.75 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. 0 mJ/cm² (B) ROS analyzed by ELISA in cells irradiated by CO₂ lattice. Data are shown as mean ± SEM.** P< 0.05 vs. 0 mJ/cm² (C) SOD expression analyzed by ELISA in cells irradiated by CO₂ lattice laser. Data are shown as mean ± SEM.** P< 0.05 vs. 0 mJ/cm² (D) MDA expression analyzed by ELISA in cells irradiated by CO2 lattice laser. Data are shown as mean ± SEM.** P< 0.05 vs. 0 mJ/cm² (E, F) Western blotting and RT-PCR of SMAD3 in cells treated with 0, 1.25, 3.75 and 6.25 mJ/cm² CO₂ Lattice Laser; ** P< 0.05 vs. 0 mJ/cm².

  
  
  

  

  CO₂ lattice laser suppresses cell senescence induced by UVB. (A) Proliferation of fibroblasts treated with control, UVB, or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (B) ELISA of ROS production in cells irradiated by control, UVB, or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (C) ELISA of SOD in cells irradiated by control, UVB or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (D) ELISA of MDA in cells irradiated by control, UVB or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB (E) Cell cycle analyzed by flow cytometry after treatment with control, UVB or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (F) Apoptosis was detected by Annexin V-PI after treatment with control, UVB or UVB and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (G, H) Expression of SMAD3, CDK4, Bcl-2, and COL1 analyzed by western blotting and RT-PCR. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB.

  
  
  

  

  CO2 Lattice Laser Reduces Cell Senescence through SMAD3. (A) Proliferation of fibroblasts treated with control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. si-SMAD3. (B) ROS production in cells irradiated by control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. si-SMAD3. (C) MDA expression in cells irradiated by control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. si-SMAD3. (D) SOD expression in cells irradiated by control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. si-SMAD3. (E, F) Expression of SMAD3, CDK4, Bcl-2, and COL1 analyzed by western blotting and RT-PCR in cells treated with control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. si-SMAD3.

  
  
  

  

  Therapeutic effect of CO₂ lattice laser on photoaging of rat skin. (A) HE staining of skin structures in control, UVB irradiation, and CO₂ lattice laser treatment groups. (B) Dermal thickness in control, UVB irradiation, and CO₂ lattice laser treatment groups. Data are shown as mean ± SEM;** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (C) ROS production analyzed by ELISA in cells irradiated by control, UVB, or UVB and 50 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (D) ELISA of MDA in cells irradiated by control, UVB or UVB and 50 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (E) ELISA of SOD in cells irradiated by control, UVB or UVB and 50 mJ/cm² CO₂ Lattice Laser. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB. (F, G) Expression of SMAD3, CDK4, Bcl-2, and COL1 analyzed by western blotting and RT-PCR in control, si-SMAD3 or si-SMAD3 and 6.25 mJ/cm² CO₂ Lattice Laser groups. Data are shown as mean ± SEM.** P< 0.05 vs. control, ## P< 0.05 vs. UVB.

  
  
  

• Research Paper Volume 8, Issue 3 pp 484-505

  MicroRNA-15b regulates mitochondrial ROS production and the senescence-associated secretory phenotype through sirtuin 4/SIRT4

  Relevance score: 3.7233112

  Alexander Lang, Susanne Grether-Beck, Madhurendra Singh, Fabian Kuck, Sascha Jakob, Andreas Kefalas, Simone Altinoluk-Hambüchen, Nina Graffmann, Maren Schneider, Antje Lindecke, Heidi Brenden, Ingo Felsner, Hakima Ezzahoini, Alessandra Marini, Sandra Weinhold, Andrea Vierkötter, Julia Tigges, Stephan Schmidt, Kai Stühler, Karl Köhrer, Markus Uhrberg, Judith Haendeler, Jean Krutmann, Roland P. Piekorz

  Keywords: MicroRNA-15b/miR-15b, nuclear encoded mitochondrial genes, photoaging, reactive oxygen species/ROS, senescence, senescence associated secretory phenotype/SASP, SIRT4/Sirtuin 4, skin

  Published in Aging on February 26, 2016

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  Mammalian sirtuins are involved in the control of metabolism and life-span regulation. Here, we link the mitochondrial sirtuin SIRT4 with cellular senescence, skin aging, and mitochondrial dysfunction. SIRT4 expression significantly increased in human dermal fibroblasts undergoing replicative or stress-induced senescence triggered by UVB or gamma-irradiation. In-vivo, SIRT4 mRNA levels were upregulated in photoaged vs. non-photoaged human skin. Interestingly, in all models of cellular senescence and in photoaged skin, upregulation of SIRT4 expression was associated with decreased levels of miR-15b. The latter was causally linked to increased SIRT4 expression because miR-15b targets a functional binding site in the SIRT4 gene and transfection of oligonucleotides mimicking miR-15b function prevented SIRT4 upregulation in senescent cells. Importantly, increased SIRT4 negatively impacted on mitochondrial functions and contributed to the development of a senescent phenotype. Accordingly, we observed that inhibition of miR-15b, in a SIRT4-dependent manner, increased generation of mitochondrial reactive oxygen species, decreased mitochondrial membrane potential, and modulated mRNA levels of nuclear encoded mitochondrial genes and components of the senescence-associated secretory phenotype (SASP). Thus, miR-15b is a negative regulator of stress-induced SIRT4 expression thereby counteracting senescence associated mitochondrial dysfunction and regulating the SASP and possibly organ aging, such as photoaging of human skin.

  

  (A) Concomitant upregulation of SIRT4 and p21^WAF expression during replicative senescence. Human foreskin fibroblast lines (from n=4 donors; mean ± s.d.) were analysed at increasing passage numbers for SIRT4 and p21^WAF mRNA levels by quantitative real-time polymerase chain reaction (qRT-PCR; suppl. Material & Methods). To evaluate statistical significance, ANOVA (on ranks for SIRT4) SNK were performed (*p<0.05). (B) Primary human dermal fibroblasts (n=4 donors; mean ± s.d.) were subjected to repetitive ultraviolet irradiation (100 J/m² UVB per day) or infrared irradiation (360 J/m² UVB per day) for a total of five days. Cells were harvested 24 and 72 h following the last irradiation and SIRT4 mRNA levels were determined by qRT-PCR. To evaluate statistical significance ANOVA on ranks (SNK) were performed (*p<0.05).

  
  
  

  

  (A) Increased SIRT4 mRNA levels in MCF7 cells driven into premature senescence through shRNA-mediated depletion of the centrosomal protein TACC3 [22] (analysis on day 4 upon doxycycline treatment which induces control or TACC3 shRNA expression; mean ± s.d. from three independent experiments). (B) Upregulation of SIRT4 mRNA levels in MCF7 cells 2, 4 and 6 days following γ-irradiation (single dose of 20 Gy; mean ± s.d. from three independent experiments). mRNA levels were determined by quantitative real-time polymerase chain reaction. To evaluate statistical significance, ANOVA SNK were performed (***p<0.001).

  
  
  

  

  (A) Subcellular visualization of MTCO2 (green) and SIRT4 (red) in γ-irradiated (20 Gy) fibroblasts as compared to control (sham treated) cells. (B) Relative quantification of total MTCO2 and SIRT4 signal intensities in γ-irradiated cells as compared to control (sham treated) cells using the ImageJ software. (C) Total SIRT4 signal intensities were normalized to MTCO2 signals in γ-irradiated cells as compared to control (sham treated) cells. Mean ± s.d. from four independent experiments. Thirty to fifty cells were analysed per experiment and condition. To evaluate statistical significance, Mann-Whitney rank sum test was performed (*p<0.05). (D) ELISA-based quantification of relative SIRT4 protein levels (suppl. Material & Methods) in γ-irradiated fibroblasts as compared to sham treated cells. As comparison, relative SIRT4 levels were determined in HEK293 cells stably expressing SIRT4-eGFP vs. eGFP expressing control cells. To evaluate statistical significance, Mann-Whitney rank sum test was performed (n=5 independent experiments, mean ± s.d).

  
  
  

  

  (A) Decreased miR-15b mRNA levels in MCF7 cells following induction of senescence through TACC3 depletion (analysis on day 4 of doxycycline-induced TACC3 shRNA expression; mean ± s.d. from three independent experiments). To evaluate statistical significance, ANOVA SNK were performed (**p<0.01). (B) Analysis of miR-15b levels in MCF7 cells following ionizing radiation (application of 20 Gy at day 0; mean ± s.d. from three independent experiments). (C) Primary human dermal fibroblasts (n=4 donors) were subjected to ultraviolet irradiation (100 J/m² UVB per day) for a total of five days. Cells were harvested 24 and 72 h following the last irradiation and miR-15b levels were determined by qRT-PCR (mean ± s.d.). To evaluate statistical significance in (b) and (c), t-tests (n=3; **p<0.01) and Mann-Whitney rank sum tests (n=4; *p<0.05) were performed, respectively.

  
  
  

  

  (A) SIRT4 expression analysis in human skin samples obtained from neck vs. buttock skin of the same individuals (age ranges: 18-25 years and 60-66 years; n=15-16 per group). (B) miR-15b expression analysis in human skin samples obtained from neck vs. buttock skin of the same individuals (age ranges: 18-25 years and 60-66 years; n=9-10 per group). (C, D) Determination of SIRT4 mRNA (c) and miR-15b (d) copy numbers in the epidermal (SIRT4: n=20; miR-15b: n=20) and dermal (SIRT4: n=12-14; miR-15b: n=17-19) compartments isolated from human photoaged skin (neck vs. buttock) of the same individuals (age range: 60-66 years). Median ± SEM; *p<0.05. To evaluate statistical significance, Wilcoxon signed rank tests were employed.

  
  
  

  

  Concomitant upregulation of SIRT4 expression (A) and downregulation of miR-15b levels (B) in human dermal fibroblasts two, four, and six days upon γ-irradiation (single dose of 20 Gy; n=6, mean ± s.d.). To evaluate statistical significance, ANOVA on ranks were performed (*p<0.05). (C) Extrinsically applied miR-15b mimics inhibit the senescence-associated upregulation of SIRT4 mRNA levels in human dermal fibroblasts upon γ-irradiation (single dose of 20 Gy) as compared to irradiated cells transfected with control mimics (n=5 independent experiments, mean ± s.d.). To evaluate statistical significance, ANOVA SNK were performed (**p<0.01).

  
  
  

  

  (A) Modulation of SIRT4 expression via transfection of miR-15b inhibitors in the absence or presence of siRNA duplexes against SIRT4 (mean ± s.d. from nine to twelve experiments). (B) ELISA-based quantification of relative SIRT4 protein levels (suppl. Material & Methods) in fibroblasts transfected with miR-15b inhibitors in the absence or presence of siRNA duplexes against SIRT4 (mean ± s.d. from four experiments). To evaluate statistical significance, ANOVA SNK was performed. (C) Confocal microscopy-based visualization of the mitochondrial marker MTCO2 (green) and SIRT4 (red) in miR-15b inhibitor-transfected fibroblasts as compared to control cells. Total SIRT4 signal intensities were normalized to MTCO2 in miR-15b inhibitor-transfected cells in the absence (D) or presence (E) of siRNA duplexes against SIRT4 using ImageJ software. Mean ± s.d. from four (D) and three (E) independent experiments. Thirty to fifty cells were analysed per experiment and condition. To evaluate statistical significance, ANOVA on ranks Dunn´s tests were performed (*p<0.05).

  
  
  

  

  Mitochondrial ROS levels (A) and the mitochondrial membrane potential (B) were determined by staining with cell-permeable dyes and flow cytometric analysis as described in Materials & Methods and by Kalfalah et al. [102]. Shown are mean ± s.d. values from four to six experiments. (C) Mitochondrial ROS levels were determined in the presence of the mitochondria-specific antioxidant mitoQ [72]. Cells were analyzed four days following transfection of miR-15b inhibitors in the absence or presence of siRNA duplexes against SIRT4. Depicted are mean ± s.d. values from four to six experiments. To evaluate statistical significance, ANOVA on ranks Dunn´s tests were performed (*p<0.05; ***p<0.001).

  
  
  

  

  Human dermal fibroblasts were transfected with control oligos (A) or miR-15b inhibitor oligos in the absence (B) or (C) presence of siRNA duplexes against SIRT4. Four days later, cells were stained with SIRT4 and MTCO2 specific antibodies. Confocal laser scanning microscopy and an ImageJ macro were employed to analyse fold changes in mitochondrial morphology-related parameters, including %area (total mitochondrial area/total cell area), mitochondrial perimeter, circularity, and solidity. Approximately two hundred cells were analysed per experimental condition. To evaluate statistical significance, ANOVA SNK were performed (*p<0.05). Bar: 20 μm.

  
  
  

  

  Inhibitors against miR-15b were transfected in primary human dermal fibroblasts in the absence or presence of siRNA duplexes against SIRT4. Transcript levels of CytC (A), TFAM (B), and NRF1 (C) were determined by qRT-PCR. Shown are mean ± s.d. values from nine to thirteen experiments. To evaluate statistical significance, ANOVA on ranks Dunn´s tests were performed (*p<0.05).

  
  
  

  

  Inhibitors against miR-15b were transfected in primary human dermal fibroblasts in the absence or presence of siRNA duplexes against SIRT4. Transcript levels of Interleukin-6 (IL-6) (A), Interleukin-8 (IL-8) (B), Interleukin-1α (IL1α) (C), Interleukin-1β (IL1β) (D), Interferon γ (IFNγ) (E), vascular endothelial growth factor (VEGF) (F), and matrix metalloproteinase-1 (MMP1) (G) were analysed by qRT-PCR. Shown are mean ± s.d. values from nine to thirteen experiments (except C, D, and E, where 5-6 independent experiments were performed). To evaluate statistical significance, ANOVA on ranks Dunn´s tests were performed (*p<0.05).